Wieschaus E, Nusslein-Volhard C, Kluding H
Dev Biol. 1984 Jul;104(1):172-86. doi: 10.1016/0012-1606(84)90046-0.
Embryos homozygous for Krüppel die as late embryos with an altered segmentation pattern. In strong alleles the normal thoracic and anterior abdominal segments are replaced by a partial mirror image duplication of the posterior abdomen. Weak alleles cause smaller pattern deletions in the thorax and abdomen and are not associated with mirror image duplications. The altered segmentation pattern can be traced back to 12 min after the onset of gastrulation, when the shorter germ bands in homozygous Kr embryos provide a first indication of abnormal patterning. The mutant was mapped to position 107.6 at the tip of the right arm of the second chromosome, cytologically to bands 60F2-5. Analysis of homozygous deficiency embryos indicate that the phenotype produced by strong point mutations probably represents the amorphic condition. The requirement for Kr+ gene activity is strictly zygotic. Maternal dosage of Kr+ has no effect on the embryonic phenotype, nor does homozygosity for Kr prevent germ cells from making normal eggs capable of normal embryonic development when fertilized by wild-type sperm. The requirement for Kr+ seems restricted to embryogenesis. Homozygous clones induced in imaginal discs during larval development survive and develop normally and in vivo cultures established from homozygous embryos proliferate normally and metamorphose into adult structures of normal morphology.
Krüppel基因纯合的胚胎在晚期胚胎阶段死亡,且具有改变的体节模式。在强等位基因中,正常的胸段和前腹段被后腹部的部分镜像重复所取代。弱等位基因会导致胸段和腹段出现较小的模式缺失,且与镜像重复无关。这种改变的体节模式可以追溯到原肠胚形成开始后的12分钟,此时纯合Krüppel胚胎中较短的胚带首次显示出异常模式。该突变体被定位到第二条染色体右臂末端的107.6位置,细胞学上位于60F2 - 5带。对纯合缺失胚胎的分析表明,强点突变产生的表型可能代表了无义状态。对Krüppel +基因活性的需求严格是合子性的。Krüppel +的母本剂量对胚胎表型没有影响,当由野生型精子受精时,Krüppel纯合也不会阻止生殖细胞产生能够正常胚胎发育的正常卵子。对Krüppel +的需求似乎仅限于胚胎发生。在幼虫发育期间在成虫盘诱导的纯合克隆能够存活并正常发育,从纯合胚胎建立的体内培养物能够正常增殖并变态为正常形态的成虫结构。